NEW YORK, Jul 01 (Reuters Health) -- An enzyme that inhibits the growth of cells
that play a role in rheumatoid arthritis has been discovered by a team of
Japanese researchers.

What's more, by genetically engineering joint cells to produce the enzyme, the
scientists were able to suppress arthritis-like symptoms in laboratory rats,
according to a report in the July issue of Nature Medicine.

If researchers can find a way to stimulate production of the enzyme in humans,
it "may provide a new approach to the effective treatment of rheumatoid
arthritis," according to Dr. Hitoshi Kohsaka and colleagues of the Tokyo
Medical and Dental University.

Rheumatoid arthritis is an
autoimmune disorder that most often strikes women between 36 and 50, and is
characterized by the infiltration of joints by inflammatory cells, leading to
swelling, and cartilage and bone destruction.

According to the report, Kohsaka and colleagues discovered that when the growth
of synovial fibroblasts -- cells lining joints -- is inhibited, the cells
continue to produce an enzyme named p16(INK4a). This enzyme is known to be
involved in cell senescence, or aging.

To duplicate the cell growth-inhibiting process, the researchers attached a
16(INK4a)-producing gene to a virus, and then used the virus to infect the
synovial fibroblasts of rats.

The forced production of extra p16(INK4a) by the joint cells "suppressed
proliferation of the rheumatoid synovial cells," Kohsaka told Reuters
Health. In rats with the arthritis-like condition, the treated joints also
showed less infiltration by inflammatory cells and less cartilage and bone
destruction compared with untreated joints.

"Our method is the first
gene therapy to transform synovial cells per se," Kohsaka told Reuters
Health. "Also, this is the first report that
cell-cycle regulator genes can be therapeutic targets of rheumatoid
arthritis."

Most importantly, the results suggest that powerful antirheumatoid arthritis
drugs could be developed that stimulate production of
p16(INK4a) in the synovial cells of humans, Kohsaka said. Such a method may also
be useful in treating other ailments caused by the abnormal proliferation of
connective tissue, according to an editorial by Drs. Dennis A. Carson and Norio
Haneji, of the University of California, San Diego. Such illnesses include
atherosclerosis, liver cirrhosis, and chronic kidney and lung diseases, they
note.

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